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Effect of wortmannin on endothelial cell proliferation and migration induced by high glucose Müller cell conditioned medium / 中华病理学杂志
Chinese Journal of Pathology ; (12): 229-232, 2005.
Artículo en Chino | WPRIM | ID: wpr-265143
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of wortmannin on endothelial cells proliferation and migration induced by high glucose Müller cell conditioned medium (HGMCM).</p><p><b>METHODS</b>Immunofluorescence, flow cytometry and Boyden chamber migration models were used to analyze the effect of wortmannin on endothelial cells.</p><p><b>RESULTS</b>50 nmol/L wortmannin could significantly inhibit the proliferation and migration of endothelial cells induced by HGMCM. The percentage of endothelial cells in S phase was obviously decreased [from (37.82 +/- 0.57)% to (21.91 +/- 0.23)%, P < 0.01], while there was an increase in the percentage of cells in G(0)/G(1) phase [from (54.57 +/- 1.19)% to (65.59 +/- 0.41)%, < 0.01] and G(2)/M phase (< 0.05).</p><p><b>CONCLUSION</b>Wortmannin can inhibit proliferation and migration of endothelial cells induced by HGMCM, suggesting that wortmannin carries an anti-angiogenetic ability in diseased retina.</p>
Asunto(s)
Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Retina / Ciclo Celular / Movimiento Celular / Células Cultivadas / Medios de Cultivo Condicionados / Fosfatidilinositol 3-Quinasas / Biología Celular / Células Endoteliales / Proliferación Celular Límite: Animales / Femenino / Humanos / Masculino Idioma: Chino Revista: Chinese Journal of Pathology Año: 2005 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Farmacología / Retina / Ciclo Celular / Movimiento Celular / Células Cultivadas / Medios de Cultivo Condicionados / Fosfatidilinositol 3-Quinasas / Biología Celular / Células Endoteliales / Proliferación Celular Límite: Animales / Femenino / Humanos / Masculino Idioma: Chino Revista: Chinese Journal of Pathology Año: 2005 Tipo del documento: Artículo